Activation of VIP signaling enhances immunosuppressive effect of MDSCs on CMV-induced adaptive immunity

• Type of Material: Article
• Authors: Parvin Forghani, Emory University; Christopher T. Petersen, Emory University; Edmund Waller, Emory University
• Language: English
• Date: 2017-10-10
• Publisher: Impact Journals
• Publication Version: Final Published Version
• Copyright Statement: © Forghani et al.
• License: Creative Commons Attribution 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.18632/oncotarget.20704
• Title of Journal or Parent Work: Oncotarget
• ISSN: 1949-2553
• Volume: 8
• Issue: 47
• Start Page: 81873
• End Page: 81879
• Grant/Funding Information: This study was funded by a generous contribution from the Abraham J. & Phyllis Katz Foundation (PI: Waller).
• Keywords: MODEL; TROPHOBLAST CELLS; VIP; CMV; mice; MICE; Immunity; Immune response; Science & Technology; myeloid-derived suppressor cells (MDSC); TUMOR MICROENVIRONMENT; Life Sciences & Biomedicine; BREAST-CANCER; Oncology; Immunology and Microbiology Section; VASOACTIVE-INTESTINAL-PEPTIDE; Cell Biology; IMMUNOMODULATION; TOLERANCE; SUPPRESSOR-CELLS
• Research Categories: Health Sciences, General; Health Sciences, Oncology; Health Sciences, Medicine and Surgery

Abstract

Vasoactive intestinal peptide (VIP) is recognized as a potent anti-inflammatory factor which affects both the innate and adaptive arms of the immune system. These effects include, but are not limited to, inhibition of T cell proliferation and disruption of immune homeostasis. Myeloid-derived suppressor cells (MDSC) are an immune regulatory cell type that has been described in settings of cancer and infectious disease. Here we demonstrate a reduced circulating monocytic MDSCs in the VIP -/- vs. wild type MCMV. VIP-/- MDSCs secretes less NO upon stimulation with LPS and interferon that relatively lose the ability to suppress T cells activation in vitro compared to wild type MDSCs. Considering the importance of VIP in immunomodulation, the possible effect of VIP in the suppressive function of MDSC populations following CMV infection remains unknown. We describe the possible role of VIP in the regulation of anti-CMV activity of T cells through the activation of MDSCs.